Abstract
An accelerating tachycardia ending in fibrillation can be initiated in isolated hearts by injections of KCl after the administration of epinephrine, but not in untreated hearts. KCl acts in two ways to do this. First, it causes an A-V block that enables epinephrine to cause a paroxysmal ventricular tachycardia. Secondly, it causes the latter to accelerate by delaying the recovery of excitability so that at least one premature systole can fall into the recovery phase of a preceding impulse. This event is necessary and sufficient for the initiation of a self-sustaining accelerating tachycardia that can end in fibrillation.